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Utilize mammalian transgenic models to examine the development and progression of breast cancer. Specifically, I use cancer prone mice (Wnt1 expression and/or Apc deficiency) to investigate evolution of primary growth and relapse in breast tumors. The mechanisms of evolution include: linking genetic constraints to carcinogen-induced tumor initiation, oncogene dose dependency, and cellular dynamics within a tumor.
June 2012 - present
- Cancer Biology/Genetics Thesis Project
- We use transgenic murine model systems to investigate the development and progression of breast cancer-- specifically Wnt-driven tumorigenesis.
Targeted cancer therapeutics select for drug-resistant rescue subclones (RSCs), which typically carry rescue mutations that restore oncogenic signaling. Whereas mutations underlying antibiotic resistance frequently burden drug-naive microbes with a fitness cost, it remains unknown whether and how rescue mutations underlying cancer relapse encounter...
Carcinogen exposures inscribe mutation patterns on cancer genomes and sometimes bias the acquisition of driver mutations toward preferred oncogenes, potentially dictating sensitivity to targeted agents. Whether and how carcinogen-specific mutation patterns direct activation of preferred oncogenes remains poorly understood. Here, mouse models of bre...
The goal of this project was to determine how mutation signatures influence driver oncogene selection. We used mutagen exposures in two distinct mouse models and determined that a carcinogen's preferred DNA damage site as well as strand-specific repair influenced Hras or Braf driver gene selection.
The second portion of my PhD project focuses on the evolution of relapse-initiating subclones in mouse models of breast cancer. Specifically, I utilize transgenic models to elucidate how oncogene overdose influences tumor evolution towards therapy-resistant relapse.